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Nickel transport by the thermophilic acetogen Acetogenium kivui

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Exogenous 63Ni was incorporated into carbon monoxide dehydrogenase when Acetogenium kivui ATCC 33488 was cultivated in the presence of 63NiCl2. The capacity for nickel (63NiCl2) transport was greatest with cells harvested from the mid- to late exponential phases of growth. Nickel transport was linear during the transport assay period and displayed saturation kinetics. The apparent Km and Vmax for nickel transport by H2-cultivated cells approximated 2.3 microM Ni and 670 pmol of Ni transported per min per mg (dry weight) of cells, respectively. The nickel transport system was not appreciably affected by the other divalent cations that were tested, and transported nickel was not readily exchangeable with exogenous nickel. Nickel transport was stimulated by glucose or H2 and was decreased by various metabolic inhibitors; however, nickel uptake by glucose- and H2-cultivated cells displayed differential sensitivities to ATPase inhibitors.
Title: Nickel transport by the thermophilic acetogen Acetogenium kivui
Description:
Exogenous 63Ni was incorporated into carbon monoxide dehydrogenase when Acetogenium kivui ATCC 33488 was cultivated in the presence of 63NiCl2.
The capacity for nickel (63NiCl2) transport was greatest with cells harvested from the mid- to late exponential phases of growth.
Nickel transport was linear during the transport assay period and displayed saturation kinetics.
The apparent Km and Vmax for nickel transport by H2-cultivated cells approximated 2.
3 microM Ni and 670 pmol of Ni transported per min per mg (dry weight) of cells, respectively.
The nickel transport system was not appreciably affected by the other divalent cations that were tested, and transported nickel was not readily exchangeable with exogenous nickel.
Nickel transport was stimulated by glucose or H2 and was decreased by various metabolic inhibitors; however, nickel uptake by glucose- and H2-cultivated cells displayed differential sensitivities to ATPase inhibitors.

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